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DOI 10.1007/s00134-016-4307-6
Abstract
Purpose: The management of peritonitis in critically ill patients is becoming increasingly complex due to their
changing characteristics and the growing prevalence of multidrug-resistant (MDR) bacteria.
Methods: A multidisciplinary panel summarizes the latest advances in the therapeutic management of these critically ill patients.
Results: Appendicitis, cholecystitis and bowel perforation represent the majority of all community-acquired infections,
while most cases of healthcare-associated infections occur following suture leaks and/or bowel perforation. The microorganisms involved include a spectrum of Gram-positive and Gram-negative bacteria, as well as anaerobes and fungi.
Healthcare-associated infections are associated with an increased likelihood of MDR pathogens. The key elements
for success are early and optimal source control and adequate surgery and appropriate antibiotic therapy. Drainage,
debridement, abdominal cleansing, irrigation, and control of the source of contamination are the major steps to ensure
source control. In life-threatening situations, a "damage control" approach is the safest way to gain time and achieve
stability. The initial empirical antiinfective therapy should be prescribed rapidly and must target all of the micro-organisms likely to be involved, including MDR bacteria and fungi, on the basis of the suspected risk factors. Dosage adjustment needs to be based on pharmacokinetic parameters. Supportive care includes pain management, optimization of
ventilation, haemodynamic and fluid monitoring, improvement of renal function, nutrition and anticoagulation.
Conclusions: The majority of patients with peritonitis develop complications, including worsening of pre-existing
organ dysfunction, surgical complications and healthcare-associated infections. The probability of postoperative complications must be taken into account in the decision-making process prior to surgery.
Keywords: Peritonitis, Source control, Multidrug-resistant bacteria, Fungal infection, Postoperative complications,
Intra-abdominal hypertension
Introduction
Despite the considerable improvement in perioperative care and empirical antibiotic therapy over recent
*Correspondence: philippe.montravers@aphp.fr
1
APHP, CHU BichatClaude Bernard, Dpartement dAnesthsie
Ranimation, Universit Denis Diderot, PRESS Sorbonne Cit, Paris, France
Full author information is available at the end of the article
Take-home message: Critically ill patients with peritonitis require an
early combined operative and medical approach. The key elements
for success are appropriate anti-infective therapy (in terms of the
most appropriate drug, at an adequate dosage with satisfactory tissue
penetration to target the microorganisms concerned) and early and
optimal source control and adequate surgery, comprising a damage
control approach in life-threatening situations.
Goal
Manoeuvre
Initial
Severity assessment
Sepsis containment
Wound protection
Microbiological diagnosis
Peritoneal cultures
Peritonitis assessment
Source control
Simple closure
Source control
1st
2nd
Resectionintestinal anastomosis
Stoma
Decrease peritoneal inoculum
3rd
Abdominal closure
Final
Organspecific management
The concepts of adequate, inadequate and difficult types
of source control depend on the specific organ constituting the source of infection (Table 2). Fresh, small
perforated duodenal ulcer is best treated by laparoscopyassisted intracorporeal suture closure. In protracted peritonitis secondary to large, chronic and/or friable peptic
ulcers in an unstable patient, quick and safe open repair
via a conservative midline incision may suffice [24, 25].
As a result of the serious consequences of protracted
infection after bariatric surgery, considerable attention
has been recently paid to early detection and treatment
(either laparoscopic or endoscopic) of any leaks [26].
Peritonitis due to small bowel perforation is not
uncommon. In faecal peritonitis or when a damage control open-abdomen technique has been used, primary
anastomosis should be delayed until improvement of the
peritoneal compartment and the patients general condition. In such circumstances, the principles of damage
control surgery with temporary ostomy should prevail
[27]. The most common abdominal source after complicated appendicitis is probably colorectal [6]. Complicated
diverticulitis is the leading cause of colonic peritonitis.
Radical source control (Hartmanns procedure) from
perforated, laparoscopic washout and intra-abdominal
drainage has raised much attention as a low-grade, easy,
straightforward approach to source control [28]. Recent
evidence is clearly against less invasive procedures in
patients with complicated diverticulitis and diffuse peritonitis [29, 30]. This policy should also be applied to leaks
following colorectal surgery with temporary ostomy.
Management ofpostoperative complications
Surgical operations can cause significant morbidity and
mortality as a result of postoperative complications [16,
17]. Peritonitis may decompensate and worsen pre-existing organ dysfunction, resulting in increased mortality.
More than 70% of these patients develop complications
[16]. The probability of postoperative complications
must be taken into account in the decision-making process prior to surgery. Several scoring systems have been
proposed to predict complications, but with disappointing results [2, 16, 17, 31]. Table 3 presents an overview
of surgical and non-surgical complications in peritonitis
and their frequency.
An association is very commonly observed between
the characteristics of the initial surgical procedure and
postoperative surgical complications [16, 17, 32]. Surgical site infections (SSI), among the most common surgical complications, are associated with the extent of stool
contamination of the wound, surgical techniques and
the patients comorbidities [17]. Superficial and deep
SSI must be treated by incision and drainage. Organ/
space SSI require more intensive intervention (CTguided drainage, relaparotomy), as SSI are usually a sign
of an occult intra-abdominal problem such as anastomotic leak. Rectal stump insufficiency, dehiscence of the
abdominal fascia and colostomy are less common complications of emergency surgery and can be repaired by
limited invasive procedures.
Surgical complications usually require reoperation.
The extent of source control interventions for complications varies substantially: from incision and drainage of a
superficial surgical site infection to CT-guided drainage
of an intra-abdominal abscess and relaparotomy comprising various types of surgical interventions. The surgical
procedure may range from simple lavage to resection of
parts of the small or large bowel and may require temporary or permanent ileostomy or colostomy, possibly leaving the abdomen open.
The role of an open abdomen technique in the management of severe peritonitis remains controversial [33]. The
abdominal contents are exposed and bowel loops are protected by placement of the omentum majus or a specific
artificial layer and a vacuum sponge. Temporary coverage
usually comprises negative pressure devices (maximum
negative pressure of minus 75mmHg) to prevent abdominal compartment syndrome (ACS) and allows a re-look
every 2448h.
Tertiary peritonitis is persistent intra-abdominal infection without a surgically treatable focus, following previous surgery and source control [14, 31]. This form of
nosocomial peritonitis is caused by a specific spectrum of
MDR microorganisms, including enterococci, Enterobacteriaceae, pseudomonas and candida. Tertiary peritonitis does not require surgery, but only a non-contributive
reoperation can confirm the diagnosis.
A high rate of healthcare-associated infections is
observed in patients with peritonitis. Up to 30 % of
patients with abdominal sepsis develop pneumonia,
which can be associated with unplanned re-intubation,
ARDS and significant mortality rates [2]. Urinary tract
infections are documented in 28% of patients with diffuse peritonitis [2, 16].
Intraabdominal hypertension
Patients with peritonitis, especially in the presence of
organ failure, present many of the known risk factors
for intra-abdominal hypertension (IAH) [34]. The two
main determinants of increased intra-abdominal pressure (IAP) may contribute to the development of IAH
and ultimately ACS: intra-abdominal volume may be
increased as a result of ischaemia/reperfusion-related
oedema, postoperative fluid accumulation and ileus,
whereas abdominal wall compliance is decreased as a
result of surgical trauma, oedema and postoperative pain.
Accepted or adequate
Difficult/controversial management
Mesenteric ischaemia
Perforated appendicitis:
Perforated cholecystitis:
Risky or inadequate
OPEN appendectomy
Perforated appendicitis:
Colorectal
Small bowel
Appendix
Gastroduodenal
Infection source
Clinical setting
Frequency Treatment
Haemodynamic instability
++
+++
Anastomotic leakage
Rupture of stoma
Tertiary peritonitis
++
+/++
CT-guided drainage
+/++
(+)
(+)
Septic shock
Haemodynamic instability
++
Pneumonia
+++
Antibiotic therapy
(+)very rare (<1%),+rare (15%), ++common (510%), +++ very common (>10%)
All these factors, particularly fluid resuscitation and surgery, may play a role in the development of IAH.
IAH has been found to impair gut perfusion [35], causing structural changes in the gut [36] and bacterial translocation [37]. In animal studies, IAH has been found to
delay healing of colonic anastomoses (ESM Fig. S1). In
summary, IAH has multiple effects that extend beyond
the abdominal cavity.
IAH should be anticipated and IAP monitoring is
advised in patients with severe sepsis or septic shock.
When IAH develops, fluid administration should be considered carefully, as parameters such as urinary output
are unreliable to assess organ perfusion.
Adequate analgesia and removal of constrictive bandages can help to increase abdominal wall compliance.
Postoperative bleeding or fluid accumulation may accentuate IAH and ultrasound may be helpful to identify
these lesions and guide drainage. Postoperative ileus and
gut distension are other common contributors to IAH,
for which nasogastric drainage and suctioning may be
required. If these interventions are unsuccessful and ACS
ensues, abdominal decompression with open abdomen
treatment may be necessary.
In some situations, an intraoperative decision to perform temporary abdominal closure may be preferable.
Consequently, postoperative IAP monitoring is mandatory to guide subsequent abdominal closure.
Microbiological considerations
The variety of pathogens isolated in the context of peritonitis represents a limited part of gastrointestinal flora.
Culture results cannot discriminate contaminating bacteria from true pathogens. The microorganisms involved
include a spectrum of Gram-positive and Gram-negative
bacteria, as well as anaerobes and fungi, with a highly
variable mix depending on several factors including the
site of perforation (ESM Fig.S2) [3]. Gram-negative and
anaerobic bacteria are increasingly involved, ranging
from about 1520 % in gastroduodenal perforation to
about 80 % in appendicitis-related peritonitis. The proportion of cultures isolating Gram-positive bacteria does
not vary substantially according to the primary source of
perforation and remains about 3040%.
Healthcare-associated infections are associated with
an increased likelihood of pathogens with reduced susceptibility to standard (first-line) antibiotic regimens.
The term MDR therefore covers methicillin-resistant
Staphylococcus aureus, coagulase-negative staphylococci,
vancomycin-resistant enterococci, extended-spectrum
beta-lactamase (ESBL)-producing Enterobacteriaceae,
quinolone-resistant Escherichia coli, and non-fermenting
Gram-negative bacteria such as Pseudomonas aeruginosa
and Acinetobacter baumannii. Factors predisposing to
MDR bacteria include corticosteroid use, recent exposure to broad-spectrum antibiotics (less than 3months),
Coagulase-negative staphylococci
Staphylococcus aureus
None. Non-extended-spectrum beta-lactamase (ESBL)-producing strains are covered by first-line antibiotic regimen
Healthcare-associated infection, especially with length of hospital stay>5days. Recent antibiotic exposure. Chronic underlying diseases leading to immunocompromised status (e.g. due
to corticosteroid use)
None. Covered by first-line antibiotic regimen
Immunodeficiency and prolonged antibiotic exposure. Tertiary
peritonitis following failure of source control, especially in
peritonitis originating from upper GI tract perforation
Candida spp.
Gram-negative bacteria
Enterococci
Streptococci
Gram-positive bacteria
Microorganism
Selection towards Candida non-albicans spp. with dose-dependent susceptibility to fluconazole in patients with prior fluconazole exposure
Resistance considerations
Piperacillin/tazobactam
At risk of ESBL infection: imipenem or
meropenem
Biliary tract infections: piperacillin/tazobactam
Biliary tract infections and at risk of ESBL
infection: piperacillin+tigecycline
Piperacillin/tazobactam+gentamicin
2009USA [8]
2010Canada [7]
2015France [10]
Amoxicillin/clavulanate+gentamicin
or cefotaxime/ceftriaxone+metronidazole
In case of -lactams allergy: levofloxacin+gentamicin+metronidazole, or
tigecycline
Amoxicillin/clavulanate, ceftriaxone or
cefotaxime+metronidazole, ertapenem
In case of -lactams allergy: gentamicin
or aztreonam+metronidazole, tigecycline
For suspected MDR Enterobacteriaceae
ertapenem or tigecycline
2009Spain [41]
Piperacillin/tazobactam+amikacinvancomycin
Allergy to -lactams: ciprofloxacin or
aztreonam+amikacin+metronidazole+vancomycin
Or tigecycline+ciprofloxacin
Piperacillin+tigecycline
Imipenem or meropenem+teicoplanin
Imipenem or meropenem+linezolid or
daptomycin or glycopeptide
Tigecycline+ceftazidime or amikacin
Piperacillin/tazobactam or carbapenems
Allergy to -lactams: fluoroquinolones or aztreonam+metronidazolevancomycin
Piperacillin/tazobactam or imipenem,
Piperacillin/tazobactam or imipenem,
meropenem or tigecycline (+antipseumeropenem or tigecycline
domonal drug in case of septic shock)
In case of -lactam allergy: tigecycline
In case of -lactam allergy: tigecycline
Amoxicillin/clavulanate, cefuroxime+metronidazole
Fluoroquinolones+metronidazole
Healthcare-associated peritonitis
Community-acquired peritonitis
2006Belgium [42]
Expert groups
Table5 Empirical antibiotic regimens proposed inrecent guidelines forcommunity-acquired andhealthcare-associated infections
Piperacillin/tazobactam
Tigecycline
Meropenem
Imipenem/cilastatin
Ceftolozane/tazobactam+metronidazole
MRSA/VRE infections: add linezolid (not necessary for tigecycline)
Generalized infection:
piperacillin/tazobactam
Ertapenem
Moxifloxacin
Tigecycline
Healthcare-associated peritonitis
Community-acquired peritonitis
Expert groups
Table5 continued
Fig.1 Suggested approach to guide antifungal therapy in patients with peritonitis, adapted from [67]
Conclusion
Critically ill patients with peritonitis require an early
combined operative and medical approach. The key elements for success are early and optimal source control
and adequate surgery and appropriate anti-infective
therapy (in terms of the most appropriate drug, at an
adequate dosage with satisfactory tissue penetration to
target the microorganisms concerned). In life-threatening situations, a damage control approach is the safest
way to gain time and achieve stability.
Electronic supplementary material
The online version of this article (doi:10.1007/s00134-016-4307-6) contains
supplementary material, which is available to authorized users.
Author details
1
APHP, CHU BichatClaude Bernard, Dpartement dAnesthsie Ranimation,
Universit Denis Diderot, PRESS Sorbonne Cit, Paris, France. 2Department
ofInternal Medicine, Ghent University, Ghent, Belgium. 3Department ofCritical Care, University Hospital Attikon, Medical School, University ofAthens, Athens, Greece. 4Department ofGeneral, Visceral andThoracic Surgery, Klinikum
Peine, Peine, Germany. 5Department ofIntensive Care Medicine andBurn
Center, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
6
Department ofEndocrine andHead andNeck Surgery, Corporaci Sanitaria
del Parc Tauli, University Hospital, Sabadell, Barcelona, Spain. 7Emergency
andIntensive Care Department, Centro Hospitalar S. Joo EPE, Porto, Portugal.
8
Department ofSurgery, Catholic University ofSacred Heart, Policlinico A
Gemelli, Rome, Italy. 9Department ofCritical Care Medicine, Ghent University
Hospital, Ghent, Belgium. 10Burns, Trauma andCritical Care Research Centre,
The University ofQueensland, Brisbane, Australia. 11Department ofMedicine,
Faculty ofMedicine, University ofPorto, Porto, Portugal.
Compliance with ethical standards
Conflicts of interest
On behalf of all authors, the corresponding author states that there is no
conflict of interest.
Received: 27 January 2016 Accepted: 4 March 2016
References
1. Barie PS, Hydo LJ, Eachempati SR (2004) Longitudinal outcomes of intraabdominal infection complicated by critical illness. Surg Infect 5:365373.
doi:10.1089/sur.2004.5.365
2. De Waele J, Lipman J, Sakr Y, Marshall JC, Vanhems P, Barrera Groba C,
Leone M, Vincent JL (2014) Abdominal infections in the intensive care
unit: characteristics, treatment and determinants of outcome. BMC Infect
Dis 14:420. doi:10.1186/1471-2334-14-420
3. De Ruiter J, Weel J, Manusama E, Kingma WP, van der Voort PH (2009) The
epidemiology of intra-abdominal flora in critically ill patients with secondary and tertiary abdominal sepsis. Infection 37:522527. doi:10.1007/
s15010-009-8249-6
4. Montravers P, Lepape A, Dubreuil L, Gauzit R, Pean Y, Benchimol D,
Dupont H (2009) Clinical and microbiological profiles of communityacquired and nosocomial intra-abdominal infections: results of the
French prospective, observational EBIIA study. J Antimicrob Chemother
63:785794. doi:10.1093/jac/dkp005
18. Lameire N, Hoste E (2014) Whats new in the controversy on the renal/
tissue toxicity of starch solutions? Intensive Care Med 40:427430.
doi:10.1007/s00134-013-3191-6
19. KDIGO Workgroup Kidney Disease (2012) Improving Global Outcomes
(KDIGO) Acute Kidney Injury Work Group: KDIGO clinical practice guideline
for acute kidney injury. Kidney Int Suppl 2:1138. doi:10.1038/kisup.2012.1
20. Casaer MP, Van den Berghe G (2014) Nutrition in the acute phase of critical illness. New Engl J Med 370:12271236. doi:10.1056/NEJMra1304623
21. Hoffer LJ, Bistrian BR (2012) Appropriate protein provision in critical
illness: a systematic and narrative review. Am J Clin Nutr 96:591600.
doi:10.3945/ajcn.111.032078
22. Solomkin JS, Ristagno RL, Das AF, Cone JB, Wilson SE, Rotstein OD, Murphy BS, Severin KS, Bruss JB (2013) Source control review in clinical trials
of anti-infective agents in complicated intra-abdominal infections. Clin
Infect Dis 56:17651773. doi:10.1093/cid/cit128
23. Azuhata T, Kinoshita K, Kawano D, Komatsu T, Sakurai A, Chiba Y, Tanjho K
(2014) Time from admission to initiation of surgery for source control is a
critical determinant of survival in patients with gastrointestinal perforation with associated septic shock. Crit Care 18:R87. doi:10.1186/cc13854
24. Sanabria A, Villegas MI, Morales Uribe CH (2013) Laparoscopic repair
for perforated peptic ulcer disease. Cochrane Database Syst Rev.
doi:10.1002/14651858.CD004778.pub3
25. Soreide K, Thorsen K, Soreide JA (2014) Strategies to improve the
outcome of emergency surgery for perforated peptic ulcer. Br J Surg
101:e51e64. doi:10.1002/bjs.9368
26. Nguyen NT, Armstrong C (2015) Management of gastrointestinal leaks
and fistula. In: Nguyen NT, Blackstone RP, Morton JM, Ponce J, Rosenthal R
(eds) The ASMBS textbook of bariatric surgery, vol 1. Springer, New York,
pp 221227
27. Waibel BH, Rotondo MF (2012) Damage control for intra-abdominal
sepsis. Surg Clin North Am 92:243257. doi:10.1016/j.suc.2012.01.006
28. Angenete E, Thornell A, Burcharth J, Pommergaard HC, Skullman S,
Bisgaard T, Jess P, Lackberg Z, Matthiessen P, Heath J, Rosenberg J,
Haglind E (2015) Laparoscopic lavage is feasible and safe for the treatment of perforated diverticulitis with purulent peritonitis: the first results
from the randomized controlled trial DILALA. Ann Surg. doi:10.1097/
sla.0000000000001061
29. Vennix S, Musters GD, Mulder IM, Swank HA, Consten EC, Belgers EH, van
Geloven AA, Gerhards MF, Govaert MJ, van Grevenstein WM, Hoofwijk
AG, Kruyt PM, Nienhuijs SW, Boermeester MA, Vermeulen J, van Dieren
S, Lange JF, Bemelman WA (2015) Laparoscopic peritoneal lavage or
sigmoidectomy for perforated diverticulitis with purulent peritonitis:
a multicentre, parallel-group, randomised, open-label trial. Lancet
386:12691277. doi:10.1016/s0140-6736(15)61168-0
30. Schultz JK, Yaqub S, Wallon C, Blecic L, Forsmo HM, Folkesson J, Buchwald
P, Korner H, Dahl FA, Oresland T (2015) Laparoscopic lavage vs primary
resection for acute perforated diverticulitis: the SCANDIV randomized
clinical trial. JAMA 314:13641375. doi:10.1001/jama.2015.12076
31. Eckmann C, Dryden M, Montravers P, Kozlov R, Sganga G (2011) Antimicrobial treatment of complicated intra-abdominal infections and
the new IDSA guidelines? A commentary and an alternative European
approach according to clinical definitions. Eur J Med Res 16:115126
32. Eckmann C, Bassetti M (2014) Prognostic factors for mortality in
(fecal) peritonitis: back to the roots! Intensive Care Med 40:269271.
doi:10.1007/s00134-013-3155-x
33. Sartelli M, Abu-Zidan FM, Ansaloni L, Bala M, Beltran MA, Biffl WL, Catena
F, Chiara O, Coccolini F, Coimbra R, Demetrashvili Z, Demetriades D, Diaz
JJ, Di Saverio S, Fraga GP, Ghnnam W, Griffiths EA, Gupta S, Hecker A, Karamarkovic A, Kong VY, Kafka-Ritsch R, Kluger Y, Latifi R, Leppaniemi A, Lee
JG, McFarlane M, Marwah S, Moore FA, Ordonez CA, Pereira GA, Plaudis H,
Shelat VG, Ulrych J, Zachariah SK, Zielinski MD, Garcia MP, Moore EE (2015)
The role of the open abdomen procedure in managing severe abdominal
sepsis: WSES position paper. World J Emerg Surg 10:35. doi:10.1186/
s13017-015-0032-7
34. Kirkpatrick AW, Roberts DJ, De Waele J, Jaeschke R, Malbrain ML, De
Keulenaer B, Duchesne J, Bjorck M, Leppaniemi A, Ejike JC, Sugrue M,
Cheatham M, Ivatury R, Ball CG, Reintam Blaser A, Regli A, Balogh ZJ,
DAmours S, Debergh D, Kaplan M, Kimball E, Olvera C (2013) Intraabdominal hypertension and the abdominal compartment syndrome:
updated consensus definitions and clinical practice guidelines from the
35.
36.
37.
38.
39.
40.
41.
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
52.
53. Ross AL, Tharp JL, Hobbs GR, McKnight R, Cumpston A (2013) Evaluation
of extended interval dosing aminoglycosides in the morbidly obese
population. Adv Pharmacol Sci 2013:194389. doi:10.1155/2013/194389
54. Pai MP (2014) Serum and urine pharmacokinetics of tigecycline in obese
class III and normal weight adults. J Antimicrob Chemother 69:190199.
doi:10.1093/jac/dkt299
55. Liu C, Bayer A, Cosgrove SE, Daum RS, Fridkin SK, Gorwitz RJ, Kaplan SL,
Karchmer AW, Levine DP, Murray BE, Talan DA, Chambers HF (2011) Clinical practice guidelines by the Infectious Diseases Society of America for
the treatment of methicillin-resistant Staphylococcus aureus infections
in adults and children: executive summary. Clin Infect Dise 52:285292.
doi:10.1093/cid/cir034
56. Cornely OA, Bassetti M, Calandra T, Garbino J, Kullberg BJ, Lortholary O,
Meersseman W, Akova M, Arendrup MC, Arikan-Akdagli S, Bille J, Castagnola E, Cuenca-Estrella M, Donnelly JP, Groll AH, Herbrecht R, Hope WW,
Jensen HE, Lass-Florl C, Petrikkos G, Richardson MD, Roilides E, Verweij
PE, Viscoli C, Ullmann AJ (2012) ESCMID guideline for the diagnosis and
management of Candida diseases 2012: non-neutropenic adult patients.
Clin Microbiol Infect 18(Suppl 7):1937. doi:10.1111/1469-0691.12039
57. Bassetti M, Marchetti M, Chakrabarti A, Colizza S, Garnacho-Montero J,
Kett DH, Munoz P, Cristini F, Andoniadou A, Viale P, Rocca GD, Roilides
E, Sganga G, Walsh TJ, Tascini C, Tumbarello M, Menichetti F, Righi E,
Eckmann C, Viscoli C, Shorr AF, Leroy O, Petrikos G, De Rosa FG (2013) A
research agenda on the management of intra-abdominal candidiasis:
results from a consensus of multinational experts. Intensive Care Med
39:20922106. doi:10.1007/s00134-013-3109-3
58. Montravers P, Dupont H, Eggimann P (2013) Intra-abdominal candidiasis:
the guidelines-forgotten non-candidemic invasive candidiasis. Intensive
Care Med 39:22262230. doi:10.1007/s00134-013-3134-2
59. Playford EG, Eggimann P, Calandra T (2008) Antifungals in the ICU. Curr
Opin Infect Dis 21:610619. doi:10.1097/QCO.0b013e3283177967
60. Eggimann P, Pittet D (2014) Candida colonization index and subsequent
infection in critically ill surgical patients: 20years later. Intensive Care Med
40:14291448. doi:10.1007/s00134-014-3355-z
61. Leon C, Ruiz-Santana S, Saavedra P, Galvan B, Blanco A, Castro C, Balasini
C, Utande-Vazquez A, Gonzalez de Molina FJ, Blasco-Navalproto MA,
Lopez MJ, Charles PE, Martin E, Hernandez-Viera MA (2009) Usefulness
62.
63.
64.
65.
66.
67.
of the Candida score for discriminating between Candida colonization and invasive candidiasis in non-neutropenic critically ill patients: a
prospective multicenter study. Crit Care Med 37:16241633. doi:10.1097/
CCM.0b013e31819daa14
Dupont H, Guilbart M, Ntouba A, Perquin M, Petiot S, Regimbeau JM,
Chouaki T, Mahjoub Y, Zogheib E (2015) Can yeast isolation be predicted
in complicated secondary non-postoperative intra-abdominal infections?
Crit Care 19:60. doi:10.1186/s13054-015-0790-3
Cuenca-Estrella M, Verweij PE, Arendrup MC, Arikan-Akdagli S, Bille J,
Donnelly JP, Jensen HE, Lass-Florl C, Richardson MD, Akova M, Bassetti M,
Calandra T, Castagnola E, Cornely OA, Garbino J, Groll AH, Herbrecht R,
Hope WW, Kullberg BJ, Lortholary O, Meersseman W, Petrikkos G, Roilides
E, Viscoli C, Ullmann AJ (2012) ESCMID guideline for the diagnosis and
management of Candida diseases 2012: diagnostic procedures. Clin
Microbiol Infect 18(Suppl 7):918. doi:10.1111/1469-0691.12038
Tissot F, Lamoth F, Hauser PM, Orasch C, Fluckiger U, Siegemund M,
Zimmerli S, Calandra T, Bille J, Eggimann P, Marchetti O (2013) Betaglucan antigenemia anticipates diagnosis of blood culture-negative
intraabdominal candidiasis. Am J Respir Crit Care Med 188:11001109.
doi:10.1164/rccm.201211-2069OC
Leon C, Ruiz-Santana S, Saavedra P, Castro C, Ubeda A, Loza A, MartinMazuelos E, Blanco A, Jerez V, Ballus J, Alvarez-Rocha L, Utande-Vazquez
A, Farinas O (2012) Value of beta-d-glucan and Candida albicans germ
tube antibody for discriminating between Candida colonization and
invasive candidiasis in patients with severe abdominal conditions. Intensive Care Med 38:13151325. doi:10.1007/s00134-012-2616-y
Pappas PG, Kauffman CA, Andes DR, Clancy CJ, Marr KA, Ostrosky-Zeichner L, Reboli AC, Schuster MG, Vazquez JA, Walsh TJ, Zaoutis TE, Sobel
JD (2015) Clinical practice guideline for the management of candidiasis:
2016 update by the Infectious Diseases Society of America. Clin Infect
Dis. doi:10.1093/cid/civ933
Pagani JL, Revelly JP, Que YA, Eggimann P (2015) The role of biomarkers for starting antifungals in the intensive care unit. Clin Pulm Med
22:286293. doi:10.1097/CPM.0000000000000118